PRRS Immunity Unconventional, adapt strategies
New research into PRRS virus and the reaction of the immune system has helped shed light on how the immune response to PRRS is unique. Teams at the University of Minnesota, and a the University of Illinois/University of Nebraska at Lincoln have looked into the onset and booster responses to the PRRS virus. Their findings have implications on how to use PRRS vaccines most effectively.
PRRS virus immunity comes on very gradually, compared to the response to other viruses, in this case, Pseudorabies virus. Only after several weeks of virus growth in tissues did cells capable of removing virus from the pig's system begin to appear. In addition, the initial response was lower, taking up to 4 months to reach a “high” level. Vaccines appear to be more gradual than virulent field viruses in turning on the response. As a consequence, the time it takes to remove field virus from the blood stream may be reduced as compared to vaccines, but with pathologic consequences. Immune responses measured included serum neutralizing antibodies (SN titers) and gamma interferon producing cells (CMI, or cell mediated immunity).
Vaccine licensing studies revealed a similar trend in protection of pigs when challenged with field virus and the clinical response was measured. Pigs vaccinated seven days prior to homologous challenge (with a similar virus) were clinically protected compared to non-vaccinated pigs, but still had signs of infection. Pigs challenged 4 weeks after vaccination were solidly protected, as compared to pigs which were not exposed to the field virus.
“Dose and Doses” Matter
A second investigation into PRRS immunity looked at the impact of virus dose and repeat exposure (booster responses) on the CMI response to PRRS virus. The immune response was specific for the PRRS virus, as evaluated both in vivo (live pigs) and in vitro (cultured lymphocytes). Most importantly, the response was specific to the antigen used, and to the dose of virus utilized. The first detection of lymphocyte proliferation, a measure of CMI, was noted at four weeks after exposure. Note these findings were consistent with the studies noted above! The peak response detected after a first exposure was seven weeks post exposure in this study, and was maintained through 11 weeks post infection.
When the pigs in this study were booster exposed, a secondary immune response was noted! While some basic immunology texts generalize that live vaccines may not need to be booster vaccinated, actual data for the PRRS vaccine, among others, support the importance of booster vaccination to increase protection and maintain ongoing protection from exposure. The impact was noted both in the lab and in the pig itself. Protection to more unrelated viruses (heterologous immunity) also appears to be more sensitive to booster response.
Application
Timing and dose critical for successful immunization
PRRS vaccines take time to develop protective immunity — the result is timing of vaccination prior to exposure is key successfully implementing a PRRS vaccine program. “You need to determine when PRRS virus exposure is occurring, and give pigs adequate time to become protected prior to that exposure. When you do this, Ingelvac PRRS MLV vaccine can be very effective in protecting pigs from many different types of field viruses”, say Dr. Luc DuFresne, Boehringer Ingelheim Vetmedica Professional Services Veterinarian. Dr. DuFresne spent several years in a large integrated production system getting first hand knowledge of the effectiveness of pig vaccination.
Key points:
- Identify if and when PRRS virus exposure is occurring.
- Vaccinate pigs with the proper dose of vaccine in the muscle, 4 or more weeks prior to exposure (up to 6 weeks prior to seroconversion)
- Vaccinate entire populations to generate the most consistent immune response
- Measure the production and economic benefits to confirm the effect.
More information
Characteristics of the immune response of pigs to wildtype PRRS virus or to commercially available vaccines: an unconventional response. Meier WA, Wheeler J, Husmann RJ, Osorio FA. Proceedings of the American Association of Swine Practitioners, March 2000. Pp 415-418.
Cell-Mediated Immunity to Porcine Reproductive and Respiratory Syndrome Virus in Swine. Bautista EM and Molitor TW. Viral Immunology Vol 10, No 2. 1997. Pp 83-94.



